A major objective is to test further our hypothesis that PGO spikes during paradoxical sleep represent neural responses to internal alerting stimuli provided by the neural bursting of that sleep phase and that they are merely a sign of activation of the same neural network involved in alerting. The characteristics of PGO spikes produced by various external stimuli during sleep and wakefulness will be compared with those occurring spontaneously in chronically implanted cats. Furthermore, the possibility that PGO spikes and eye movement potentials are essentially similar phenomena will be examined further. A related hypothesis to be tested is that the varying degrees of insomnia produced by electrolytic lesions of the brainstem raphe nuclei are the result of the removal of an inhibitory influence on alerting mechanisms. Raphe lesions will be made, and then cats will be tested for the ease with which they can be distracted or alerted in wakefulness and PGO spikes can be induced in sleep or wakefulness. Also, effects of various specific brainstem tegmental lesions will be restudied with the hope of resolving conflicting opinions regarding their effects on paradoxical sleep behavior. In addition, connectivity of relevant brainstem structures will be studied anatomically. The phenomenon of paradoxical sleep without atonia, which can be produced by pontine lesions, will then be used to pursue further the idea that poikilothermy exists during paradoxical sleep by examining for presence or absence of the behavioral thermo-regulatory responses, such as shivering and panting during that altered sleep phase.